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Large GI > Hepatobilary, Oral cavity/esophagus, Reticulorumen > Flashcards

Hepatobilary, Oral cavity/esophagus, Reticulorumen Flashcards

1
Q

What is the etiology of liver abscesses?

A

Fusobacterium necrophorum

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2
Q

What causes rumenitis and how can it lead to liver abscesses?

A

Dairy/beef cattle on high concentrate diets, causes lactic acidosis. most common cause

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3
Q

What causes naval infections in neonates?

A

Umbilical vein predisposed to ascending infection, travels to liver.

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4
Q

What are clinical signs of liver abscesses?

A

Most are subclinical! Decreased rate of gain, weigh tloss, pyrexia, anorexia, abdominal pain (rolling).

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5
Q

What are 3 sequelae of liver abscesses?

A

Caudal vena caval thrombosis
Peritonitis
Occlusion of bile duct

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6
Q

What is the clinical pathology associated with liver abscesses?

A

Neutrophilia with left shift, hyperfibrinogenemia, hyperglobulinemia, hypoalbuminemia, elevations in GGT and AST, hyperbilirubinemia, anemia

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7
Q

Why do you see hypoalbuminemia with liver abscesses?

A

Hepatic insufficiency because of abscesses

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8
Q

What is the pathophysiology associated with liver abscesses?

A

Normal flora–>breakdown in rumen mucosa leads to acidosis (high grain diet)–>portal circulation–>abscesses form and encapsulate–>erosion of hepatic vessels–>emboli–>hematogenous pneumonia and caval syndrome

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9
Q

What do you treat liver abscesses with?

A

broad spectrum antibiotics but few penetrate

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10
Q

How can you prevent liver abscesses?

A

prevent rumenitis, feed additive antibiotics, prevent umbilical infections in calves

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11
Q

What leads to hepatic lipidosis?

A

sequelae of severe ketosis

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12
Q

What is typical signalment for hepatic lipidosis?

A

postpartum dairy cows, over-conditioned beef cows

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13
Q

Why are over-conditioned beef cows more at risk for hepatic lipidosis?

A

Don’t follow normal production cycle. Pregnant for 9 months, then 3 months to get pregnant again while recovering during that time. Overgraze when they can’t get pregnant right away.

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14
Q

What are clinical signs of hepatic lipidosis?

A

weakness–recumbency, pronounced anorexia, dec milk production, ketosis

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15
Q

What is the pathophysiology of hepatic lipidosis?

A

overfeeding in dry perioid, mobilization of adipose tissue fatty acids in response to negative energy balance

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16
Q

What are treatment goals for hepatic lipidosis?

A

Eliminate negative energy balance. Treat concurrent diseases. IV glucose infusion.

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17
Q

How can hepatic lipidosis be prevented?

A

Prevent obesity in late lactation, maintain weight during dry period.

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18
Q

What is the most common liver fluke in cattle?

A

Fasciola hepatica

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19
Q

What is the life cycle of a trematode?

A

indirect lifestyle–one egg can become amplified into multiple adults

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20
Q

_____(spp) more commonly have acute infections of liver flukes while ______ (spp) more commonly have chronic infections.

A

Sheep–acute

Cattle–chronic

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21
Q

What pathology will you see with acute vs chronic liver fluke infections?

A

Acute–hemorrhage tracts

Chronic–white fibrotic tracts

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22
Q

How do liver flukes cause major liver damage?

A

Migrate through liver to cause damage and insufficiency, cholangitis, and biliary obstruction and fibrosis.

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23
Q

Fascioloides magna is a liver fluke of ______ (spp). What effects does it have in cattle?

A

Deer.

Cattle–poor performance in cows, poor growth rate in calves.

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24
Q

Why are fascioloides magna eggs not found in a fecal?

A

Flukes wall themselves off in the body and do not become patent.

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25
Q

What is treatment for liver flukes? Why is timing important?

A 
Flukicides--strategically time these because they only target the adult form
Snail management (but how feasible is this actually?).
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26
Q

Flukicide treatment is best from ______ for the SE and ______ for the Pacific NW.

A

SE–July thru Oct

P. NW–Nov thru Dec

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27
Q

When do you see hepatotoxicity due to plants?

A

Poor management, animals will resort to eating these when good forage is unavailable.

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28
Q

When will you see clinical signs from hepatotoxicity?

A

When 75% of functional hepatic mass has been compromised.

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29
Q

What is secondary photosensitization?

A

Hepatic insufficiency inhibits adequate systemic clearance of phylooerythrin, which goes into circulation. Will see lesions on dorsal midline and non-pigmented areas, sometimes on teats (cattle cool off in ponds, reflects light back onto udder area).

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30
Q

What are some causes of “broken mouth”?

A

Older cattle
Mineral deficiencies–phosphorus, Vit D, Ca, Ricketts, osetomalasa
Toxicities–Fluoride

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31
Q

Which teeth are more commonly fractured? When will you see clinical signs?

A

Molars/premolars»incisors

Will be asymptomatic unless root is involved.

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32
Q

How do tooth root abscesses occur?

A

Infection from gingivitis or fractured teeth has spread down the tooth root.

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33
Q

What organism causes Wooden Tongue?

A

Actinobacillus lingieresii, normal inhabitant of oral cavity.

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34
Q

Where are wooden tongue lesions found?

A

SOFT TISSUE. Most often granulomas at the base of the tongue. Bacteria penetrates mucosa.

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35
Q

What is the treatment for wooden tongue?

A

Sodium iodide

36
Q

What organism causes Lumpy Jaw?

A

Actinomycosis bovis, normal inhabitant of oral cavity.

37
Q

Where are lumpy jaw lesions found?

A

Bacterium gains entrance to BONE from punctures by foreign bodies, coarse feedstuff, diseased tooth, gingivitis.

38
Q

What is the cardinal sign of lumpy jaw?

A

Hard, immovable non-painful mass on mandible. Can develop fistulous tracts that have exudate and are painful.

39
Q

What is stomatis and what are the clinical signs?

A

Inflammation of the oral cavity.

Anorexia, ptyalism, fetid breath, local lymphadenopathy.

40
Q

______ is a viral cause of stomatitis and ______ is a bacterial cause.

A

Viral–Bovine Papular Stomatitis

Bacterial–Oral Necrobacillosis (Fusobacterium necrophorum)

41
Q

What is the signalment for Bovine Papular Stomatitis?

A

Young cattle, feedlot animals within 4 weeks of arrival.

42
Q

What is the signalment for Oral Necrobacillosis?

A

Young, milk-fed calves.

43
Q

What are the hosts of Vesicular Stomatits?

A

Pigs, sheep, cattle, horse.

44
Q

How does Foot and Mouth Disease (FMD) differ from other vesicular diseases?

A

Rapidly travels through herds.

45
Q

What are the 3 primary hosts of FMD and what are their roles?

A

Sheep–maintenance hosts
Pigs–amplifiers
Cattle–indicators

46
Q

Why is choke common in cattle? What is the most common cause of it?

A

They are indiscriminate eaters.

Rapid ingestion of grain, doesn’t stimulate saliva production and causes bloat.

47
Q

What is an indicator of true bloat?

A

Will see ruminal tympany with extended upper left side of abdomen, may or may not hear ping.

48
Q

How does the chewing of cud aid in digestion?

A

Further breaks down feed and releases bacteria, which increases fermentation.

49
Q

What are the four specialized contraction patterns? Which phase causes bloat?

A
  1. primary contraction–16 steps
  2. secondary contraction–occurs every 3-5 primary contractions, pushes gas forward so cattle can eructate this phase causes bloat!
  3. rumination–chewing of cud
  4. esophageal groove closure–eversion of milk to abomasum from esophagus in calves
50
Q

What do you determine in every forestomach exam?

A

Rate/strength of contractions
Rumen volume
Nature of rumen contents
Nature of feces

51
Q

Normal ascultation of the rumen will have ____ contractions per minute.

A

2-3

52
Q

What can cause hypomotility of the rumen?

A

Decreased Ca, bloat, increased sympathetic stimulation due to “fight or flight” reflex

53
Q

What can cause hypermotility of the rumen?

A

Vagal indigestion.

54
Q

Why is it important for there to be stratification of contents in the rumen?

A

Sign of a healthy rumen, keeps them eructating like they need to.

55
Q

What are the 4 main stratifications of the rumen?

A

(top to bottom)

Gas–solid–slurry–liquid

56
Q

What is normal pH of the rumen?

A

Depends on what is fed! Grain decreases pH, fiber/forage increase pH.

57
Q

What happens as a result of vagal indigestion?

A

abdominal distention

58
Q

Type 1 vagal indigestion

A

Failure to eructate–inability to handle gas, not that there was too much produced

59
Q

Type 2 vagal indigestion

A

Failure of omasal transport–stenosis

hardware disease!

60
Q

Type 3 vagal indigestion

A

Abomasal impaction

61
Q

Type 4 vagal indigestion

A

Indigestion of advanced pregnancy. RARE.

62
Q

_______ is a major cause of vagal indigestion. What species is this most common in?

A

Hardware disease, beef cattle.

63
Q

What causes primary abomasal impaction?

A

Dry, coarse feed with restricted water access

64
Q

What causes secondary abomasal impaction?

A

Decreased abomasal emptying.

65
Q

What are the clinical signs of abomasal indigestion?

A 
"Papple" contour of abdomen
Intermittent bouts of indigestion and anorexia
Weight loss
Regurg
Poor digestion--will see stems in feces
Increased rumen contractions
L shaped rumen on rectal palpation
66
Q

What happens with chloride levels in the rumen with vagal indigestion?

A

Will be decreased in the blood, increased in the rumen. (Type 3 and 4)

67
Q

What is rumen putrefaction? What is the typical signalment?

A

Putrefactive decompistion of forestomach contents.

Milk-fed calves.

68
Q

Why does rumen putrefaction occur?

A

Poor esophageal groove function.

69
Q

What will the pH be in calves with rumen putrefaction?

A

Alkaline pH>7 in older calves with necrosis.

Acidic rumen pH<5.5 in younger calves with esophageal groove dysfunction.

70
Q

What are clinical signs of rumen putrefaction?

A

Recurrent bloat
Intermittent diarrhea
Chronic poor growth–pot belly
Rumen distended with fluid

71
Q

How does rumen tympany occur?

A

Failure of eructation

72
Q

What are causes of free gas bloat?

A

Secondary disease, esophageal dysfunction, ruminal motility dysfunction

73
Q

What are causes of frothy bloat?

A

Primary disease, relaxation of cardia does not occur

74
Q

______ are more likely to cause frothy bloat over perennial grasses.

A

Legumes

75
Q

What is treatment of frothy bloat?

A

Anti-foaming agents: poloxalene, mineral oil, docusate sodium

76
Q

How do you prevent frothy bloat?

A 
Feed dry, coarse forages before putting on legume grasses. 
Ionophores. 
Supplement pasture with dry grass hay. 
Pasture after dew has evaporated. 
Adapt to diet slowly.
77
Q

What is the most common cause of lactic acidosis?

A

Ration is changed–increased rapidly fermentable carbs (aka too much grain!)

78
Q

What is the biggest indicator on clin path of lactic acidosis?

A

Metabolic acidosis

79
Q

How do you treat lactic acidosis?

A

Remove acid-inducing feedstuffs from the rumen by oral lavage or rumenotomy.
Antacids, charcoal, fluid/electrolytes, oral thiabendazole.

80
Q

Hardware disease is technically known as ___________.

A

Traumatic reticuloperitonitis

81
Q

What occurs with hardware disease?

A

Perforation of reticulum by foreign body, contamination of body cavities or organs.

82
Q

Goats or cattle more commonly have hardware disease?

A

Cattle–indiscriminate eaters

83
Q

What are the outcomes of hardware disease?

A

Localized or diffuse peritonitis
Peri-reticular abscesses, liver abscesses
Vagal indigestion

84
Q

What kind of posture will an animal with hardware disease have?

A

Show signs of abdominal pain; elbows abducted, arched back.

85
Q

How do you diagnose hardware disease?

A

CBC (neutrophilia, leukopenia)
Fibrinogen
Peritoneal fluid exam
U/S, rads

86
Q

What are treatment options for hardware disease

A

Medical, exploratory laparotomy and rumenotomy.

87
Q

How can you prevent hardware disease?

A

Magnets on feed processing, reticular magnets.

Large GI (4 decks)

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